- Rita Allen Foundation

All Scholars

Since 1976, the Rita Allen Foundation has awarded millions of dollars in grants to early-career biomedical scholars. These grants allow Rita Allen Foundation Scholars to establish labs and pursue research directions with above-average risk and promise. See below for a full list of Scholars, or read more about the Rita Allen Foundation Scholars program.

2020

Ishmail Abdus-Saboor +
Columbia University (University of Pennsylvania)

Ishmail Abdus-Saboor

Mitchell J. and Margo K. Blutt Presidential Assistant Professor, Biology

B.S., North Carolina A&T University

Ph.D., University of Pennsylvania

In conjunction with Open Philanthropy

My research focuses on a long-standing question—how does the nervous system encode a soft gentle caress versus a harsh painful stimulation? To accomplish this, the Abdus-Saboor Lab uses neurobiology, computational biology, and mathematics to objectively measure pain—a sensory experience that is inherently subjective. Traditionally, researchers have applied sensory stimuli to the rodent paw and tried to infer the animal’s pain state based on the singular readout of whether the animal moved its paw or not. The problem is, animals will lift their paw to both innocuous and noxious stimuli; and with that sole measurement parameter, there is a high likelihood of incorrectly assigning the animal’s sensory experience. An innovation in our work is to use videography to take thousands of images per second to measure sub-second pain behaviors, and couple this with statistical modeling and machine learning to develop rodent “pain scales.”
Grace Chen +
Yale University

Grace Chen

Assistant Professor, Immunobiology

B.S., University of California, Berkeley

Ph.D., Harvard University

An essential function of the immune system is to distinguish between its own and foreign molecules in order to destroy pathogens while preventing destruction of healthy cells. The Chen Lab investigates how the immune system correctly identifies pathogens when the same signals are found in both host cells and pathogens. Circular RNAs (circRNAs)—single-stranded RNAs where the ends are joined together—are encoded by eukaryotes and viruses. We study the essential features of viral and host circRNAs that are required in the regulation and recognition of self- versus non-self, the proteins involved in this process, and the ensuing cellular signaling. We strive to apply our understanding to engineer circRNAs as a novel strategy for immunotherapy that exploits the uniquely promising characteristics of circRNAs.
Geoffroy Laumet +
Michigan State University

Geoffroy Laumet

Assistant Professor, Physiology

Ph.D., Lille University School of Medicine, France

The Laumet Lab is interested in understanding why pain becomes chronic and how can we stop it. While it is obvious that neurons convey pain signaling throughout the body, neurons do not work in isolation and are constantly communicating with and getting influenced by other cells. We are particularly interested in the contribution of non-neuronal cells to chronic pain. We think that impaired communication between “pain-sensing” neurons and their surrounding cells may result in chronic pain. For example, we have discovered that anti-inflammatory molecules secreted by cells from the immune system prevent pain-sensing neurons from becoming persistently activated—this constant activity is the cellular basis of chronic pain. We hope that a better understanding of neuron/non-neuronal cell communication will lead to the development of new and better analgesics.
Sarah Linnstaedt +
University of North Carolina at Chapel Hill

Sarah Linnstaedt

Assistant Professor, Anesthesiology

B.S., Virginia Tech

Ph.D., Georgetown University

In conjunction with Open Philanthropy

Almost all individuals will experience at least one traumatic injury in their lifetime. While the majority of these individuals recover, a substantial subset develop chronic post-traumatic pain (CPTP). The Linnstaedt Lab is interested in better understanding how to predict which individuals will recover versus develop CPTP following trauma, and how to prevent CPTP in those at high risk. To address this goal, we use translational research approaches to discover genetic and molecular vulnerability factors that predict CPTP and to identify promising targets for therapeutic preventative interventions.
Jeremy M. Rock +
The Rockefeller University

Jeremy M. Rock

Assistant Professor, Microbiology and Infectious Diseases

B.A., University of California, Berkeley

Ph.D., Massachusetts Institute of Technology

Mycobacterium tuberculosis is the leading cause of death due to infectious disease and it infects one-quarter of the world’s population. By investigating the mechanisms that enable this bacterium to cause tuberculosis and evade current antibiotics, the Rock Lab aims to lay the foundation for new therapeutic strategies to improve control of this epidemic.
Andrew J. Shepherd +
The University of Texas MD Anderson Cancer Center

Andrew J. Shepherd

Assistant Professor, Department of Symptom Research

B.S., The University of Manchester Institute of Science and Technology, United Kingdom

Ph.D., The University of Manchester, United Kingdom

Work in the Shepherd Lab focuses on how injury, inflammation, and cancer interact with the nervous system to cause pain. We are particularly interested in how chronic illnesses disrupt the immune system, thereby increasing pain risk. Macrophages, a type of immune cell, are important contributors to pain. Macrophages infiltrate damaged tissue to clear debris and infection. Ordinarily, this process eventually resolves, promoting healing. We hypothesize that chronic pain often stems from macrophages failing to make this transition from a “damage response” to a “pro-repair” state. In such cases, macrophages continually sustain inflammation, causing nearby nerves to remain hyper-excitable and drive chronic pain. Our knowledge of these mechanisms is surprisingly limited, a problem that is set to become more widespread as chronic illnesses and cancer survivorship improve. We hope that improving our understanding of these “neuro-immune” interactions will identify novel therapeutic targets and facilitate the development of safe and effective analgesics.
Tuomas Tammela +
Memorial Sloan Kettering Cancer Center

Tuomas Tammela

Assistant Member

M.D., University of Helsinki, Finland

Ph.D., University of Helsinki, Finland

Cancer cells within tumors assume distinct identities, forming diverse cellular societies. Despite this diversity, the current paradigm is to treat tumors with homogeneous cancer therapy regimens. This thinking persists despite strong evidence from preclinical models and human patients that tumors are heterogeneous and, therefore, cellular identities capable of withstanding and adapting to therapies invariably exist. The Tammela Lab seeks to understand how cancer cells acquire the ability to transition between these identities and promote intra-tumoral heterogeneity. To do this, we will use a series of innovative approaches and models of human cancer. Our hope is that these efforts will lead to conceptually new types of cancer therapies to prevent cancer cells from transitioning to treatment-resistant states.
David Van Valen +
California Institute of Technology

David Van Valen

Assistant Professor, Biology and Biological Engineering

B.S., Massachusetts Institute of Technology

M.D., University of California, Los Angeles

Ph.D., California Institute of Technology

Viruses are in constant conversation with the cells they infect, and the information exchanged can be used by the host or the virus to guide their respective behaviors. For example, viruses may decide to become dormant after infection, while host cells may choose to activate an immune response. The Van Valen Lab listens in on this conversation to understand how viruses and their hosts represent information about their internal state and their environment, and how this information is accessed to make decisions. To do so, we combine ideas from cell biology and physics with recent advances in imaging, machine learning, and genomics to make novel measurements of host–virus interactions. Active projects include imaging the interaction between host immune and metabolic signaling networks during infection, measuring host–virus interactions in a model system of viral latency, and developing novel deep-learning approaches to single-cell analysis of biological imaging data.
Amanda Whipple +
Harvard University

Amanda Whipple

Assistant Professor, Molecular and Cellular Biology

B.S., The University of Oklahoma

Ph.D., Baylor College of Medicine

Amanda Whipple has been designated the Milton E. Cassel Scholar for the 2020 class of Rita Allen Foundation Scholars. This special award honors the memory of a longtime President of the Rita Allen Foundation who passed away in 2004.

Our DNA represents the full library of genetic information each of us inherits from our parents. We inherit two copies of each gene—one from our mother and one from our father. Typically, the two copies are treated equally in the cell. However, the Whipple Lab studies a unique class of “imprinted genes,” in which only one parental copy is active (“expressed”) while the other is inactive (“silenced”). Many imprinted genes are expressed in the brain and are associated with diverse neurological disorders. Yet, the reasons for imprinted expression and the effects of imprinted gene activity in the brain remain largely unknown. We use molecular and bio-computational approaches to understand: (1) why genes evolved imprinted expression in the brain, (2) how imprinted genes function in neurons, and (3) how dysregulation of imprinted genes contributes to neurological diseases.

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